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Query: UMLS:C0011860 (type 2 diabetes)
57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ventricular dysfunction in type 2 diabetic patients is becoming apparent early after diagnosis of diabetes, but the cellular mechanisms contributing to this dysfunction are not well established. Our group has recently identified cardiomyocyte dysfunction in diet-induced insulin resistant rats that have not developed type 2 diabetes. The present investigation was designed to determine cellular mechanisms contributing to slowed cardiomyocyte relaxation in sucrose (SU)-fed rats. SU-feeding was used to induce whole-body insulin resistance. After 9-12 weeks on diet, isolated ventricular myocyte shortening/relengthening were slower in SU-fed adult male Wistar rats (42-63%) compared to starch (ST)-fed controls. Cytosolic Ca2+ removal attributable to Na+/Ca2+ exchange (NCX) and to sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) was evaluated with fluo-3/AM. Caffeine-releasable Ca2+ and cytosolic Ca2+ clearing through NCX were normal, whereas Ca2+ uptake by SERCA was significantly slower in SU myocytes (330+/-29 ms) compared to ST cells (253+/-16 ms). Protein levels for SERCA, NCX and phospholamban were not affected by SU-feeding. Manipulating intracellular Ca2+ with various positive inotropic interventions (e.g. post-rest potentiation, isoproterenol) and changes in stimulus frequency demonstrated that mechanical properties can be improved in subsets of myocytes. Thus, we conclude that impaired SERCA activity (with normal protein content) contributes to cardiomyocyte dysfunction in insulin resistant animals, whereas NCX function and expression are normal. These results suggest that subtle changes in Ca2+ regulation which occur prior to overt ventricular dysfunction/failure, may be common to early stages of a number of disorders involving insulin resistance (e.g. diabetes, obesity, syndrome X and hypertension).
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PMID:Impaired SERCA function contributes to cardiomyocyte dysfunction in insulin resistant rats. 1587 73

We systematically reviewed cohort studies on the effect of nutrient and food intake (except for alcohol) on the incidence of type 2 diabetes, which had been published in English as of May 2004. Using the MEDLINE (PubMed) database as well as reference lists of searched papers, 15 individual cohort studies (a total of 31 papers) were identified. The number of subjects (n= 895-85,060), follow-up length (5.9-23 y), the number of diabetes cases (n= 74-4,085), dietary assessment method used (simple food questionnaire, food frequency questionnaire, food frequency interview, diet history interview, and 24-h recall), and method of case ascertainment (questionnaire, oral glucose tolerance test, fasting glucose level, death certificate, and nationwide registry) varied among studies. For nutrients, intakes of vegetable fat, polyunsaturated fatty acid, dietary fiber (particularly cereal fiber), magnesium, and caffeine were significantly inversely correlated and intakes of trans fatty acid and heme-iron, glycemic index, and glycemic load were significantly positively correlated with the incidence of type 2 diabetes in several papers. For foods and food groups, several papers showed significantly decreased risk for type 2 diabetes with the higher consumption of grain (particularly whole grain) and coffee, and significantly increased risk with processed meat consumption. Because all the studies were carried out in Western countries, however, research in non-Western countries including Japan is needed.
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PMID:Effect of dietary factors on incidence of type 2 diabetes: a systematic review of cohort studies. 1626 5

Coffee consumption has been associated with improved glucose tolerance and a lower risk of type 2 diabetes in diverse populations in the U.S., Europe, and Japan. This review discusses the strength of the evidence, relevant mechanisms, possible implications, and directions for further research. The finding that higher consumption of decaffeinated coffee was associated with a lower risk of type 2 diabetes suggests that coffee constituents other than caffeine play a role. Coffee is a source of several compounds that improved glucose metabolism in animal studies, including the chlorogenic acids and lignans. Further research on phytochemicals in coffee may lead to the identification of novel mechanisms for effects of diet on the development of type 2 diabetes. In addition, knowledge on effects of coffee components may aid in the development or selection of types of coffee with improved health effects. Longer-term randomized intervention studies that test the effects of coffee consumption on glucose tolerance are warranted. Physical activity and weight management should be the mainstay of public health strategies to prevent type 2 diabetes. For individual choices regarding coffee consumption, potential effects of coffee on various health outcomes should be considered.
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PMID:Coffee and type 2 diabetes: from beans to beta-cells. 1639 94

Coffee is a complex mixture of chemicals that provides significant amounts of chlorogenic acid and caffeine. Unfiltered coffee is a significant source of cafestol and kahweol, which are diterpenes that have been implicated in the cholesterol-raising effects of coffee. The results of epidemiological research suggest that coffee consumption may help prevent several chronic diseases, including type 2 diabetes mellitus, Parkinson's disease and liver disease (cirrhosis and hepatocellular carcinoma). Most prospective cohort studies have not found coffee consumption to be associated with significantly increased cardiovascular disease risk. However, coffee consumption is associated with increases in several cardiovascular disease risk factors, including blood pressure and plasma homocysteine. At present, there is little evidence that coffee consumption increases the risk of cancer. For adults consuming moderate amounts of coffee (3-4 cups/d providing 300-400 mg/d of caffeine), there is little evidence of health risks and some evidence of health benefits. However, some groups, including people with hypertension, children, adolescents, and the elderly, may be more vulnerable to the adverse effects of caffeine. In addition, currently available evidence suggests that it may be prudent for pregnant women to limit coffee consumption to 3 cups/d providing no more than 300 mg/d of caffeine to exclude any increased probability of spontaneous abortion or impaired fetal growth.
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PMID:Coffee and health: a review of recent human research. 1650 75

Although acute alkaloid caffeine (CAF) ingestion results in an impaired glucose tolerance, chronic coffee (RCOF) ingestion decreases the risk of developing type 2 diabetes. This study examines the hypothesis that CAF ingestion impairs glucose tolerance to a greater extent than RCOF and that the ingestion of decaffeinated coffee (DECAF) results in a positive effect. Eleven healthy males underwent 4 double-blinded randomized trials. Each trial included the ingestion of either: 1) CAF in capsule form (4.45 mg/kg body weight), 2) RCOF (4.45 mg/kg body weight caffeine), 3) dextrose (placebo, PL) in capsule form, or 4) DECAF (equal in volume to the RCOF trial), followed 1-h later by a 2-h oral glucose tolerance test. Blood samples were collected at baseline (-30), 0 (time of treatment ingestion), 60 (initiation of oral glucose tolerance test), 75, 90, 120, 150, and 180 min. Area under the curve for glucose and insulin were higher (P < or = 0.05) following CAF than both PL and DECAF and, although a similar trend (P = 0.07) was observed following RCOF compared with DECAF, the effect was less pronounced. Interestingly, DECAF resulted in a 50% lower glucose response (P < or = 0.05) than PL, suggesting that the effects of PL and DECAF on glucose tolerance are not the same. These findings suggest that the effects of CAF and RCOF are not identical and may provide a partial explanation as to why acute CAF ingestion impairs glucose tolerance while chronic RCOF ingestion protects against type 2 diabetes.
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PMID:The glucose intolerance induced by caffeinated coffee ingestion is less pronounced than that due to alkaloid caffeine in men. 1661 16

The purpose of this study was to explore the association of serum caffeine concentrations with serum glucose levels in caffeine-drug users and non-users, aiming at the chronic effects of caffeine on glucose metabolism in comparison with known acute effects of caffeine. Eight hundred and fourteen caffeine-drug users and 623 non-users were identified from German National Health Surveys. Their serum caffeine concentrations and glucose levels were measured. The associations of caffeine concentrations with glucose levels were established by correlation analysis and multivariable regression analysis in caffeine-drug users and non-users separately. Antidiabetic therapy was considered. Caffeine concentrations were closely positively correlated to serum glucose levels in caffeine-drug users (Spearman r = 0.117, p = 0.001; partial r = 0.102, p = 0.020) particularly in women (Spearman r = 0.155, p < 0.001; partial r = 0.150, p = 0.005) although the correlation was weak as shown by multivariable regression analysis. The serum glucose levels were significantly higher (5.403 +/- 0.033 vs. 5.306 +/- 0.037 mmol/l) whereas the magnesium level was significantly lower (0.8941 +/- 0.0026 vs. 0.9024 +/- 0.0030 mmol/l) in caffeine-drug users than in non-users. No associations of caffeine concentrations with serum glucose levels were found in any groups of caffeine-drug non-users in our study. Whereas acute intake of caffeine-drugs may impair glucose metabolism, chronic intake of caffeine exclusively from diet has little effects on glucose metabolism and therefore may not contribute to the risk reduction of type 2 diabetes that was found in recent coffee consumption studies.
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PMID:Association of serum caffeine concentrations with serum glucose levels in caffeine-drug users and non-users - results of German National Health Surveys. 1769 66

Adenosine influences metabolism and the adenosine receptor antagonist caffeine decreases the risk of type 2 diabetes. In this study the metabolic role of one adenosine receptor subtype, the adenosine A(1)R, was evaluated in mice lacking this receptor [A(1)R (-/-)]. The HbA1c levels and body weight were not significantly different between wild type [A(1)R (+/+)] and A(1)R (-/-) mice (3-4 months) fed normal lab chow. At rest, plasma levels of glucose, insulin and glucagon were similar in both genotypes. Following glucose injection, glucose tolerance was not appreciably altered in A(1)R (-/-) mice. Glucose injection induced sustained increases in plasma insulin and glucagon levels in A(1)R (-/-) mice, whereas A(1)R (+/+) control mice reacted with the expected transient increase in insulin and decrease in glucagon levels. Pancreas perfusion experiments showed that A(1)R (-/-) mice had a slightly higher basal insulin secretion than A(1)R (+/+) mice. The first phase insulin secretion (initiated with 16.7 mM glucose) was of the same magnitude in both genotypes, but the second phase was significantly enhanced in the A(1)R (-/-) pancreata compared with A(1)R (+/+). Insulin- and contraction-mediated glucose uptake in skeletal muscle were not significantly different between in A(1)R (-/-) and A(1)R (+/+) mice. All adenosine receptors were expressed at mRNA level in skeletal muscle in A(1)R (+/+) mice and the mRNA A(2A)R, A(2B)R and A(3)R levels were similar in A(1)R (-/-) and A(1)R (+/+) mice. In conclusion, the A(1)R minimally affects muscle glucose uptake, but is important in regulating pancreatic islet function.
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PMID:A1 receptor deficiency causes increased insulin and glucagon secretion in mice. 1786 24

Epidemiological studies indicate that regular coffee consumption reduces the risk of developing type 2 diabetes. Despite these findings, the biological mechanisms by which coffee consumption exerts these effects are unknown. The aim of this study was twofold: to develop a rat model that would further delineate the effects of regular coffee consumption on glucose kinetics, and to determine whether coffee, with or without caffeine, alters the actions of insulin on glucose kinetics in vivo. Male Sprague-Dawley rats were fed a high-fat diet for 4 weeks in combination with one of the following: (i) drinking water as placebo (PL), (ii) decaffeinated coffee (2 g/100 mL) (DC), or (iii) alkaloid caffeine (20 mg/100 mL) added to decaffeinated coffee (2 g/100 mL) (CAF). Catheters were chronically implanted in a carotid artery and jugular vein for sampling and infusions, respectively. Recovered animals (5 days postoperative) were fasted for 5 h before hyperinsulinemic-euglycemic clamps (2 mU x kg(-1) x min(-1)). Glucose was clamped at 6 mmol/L and isotopes (2-deoxy-[(14)C]glucose and [3-(3)H]glucose) were administered to obtain indices of whole-body and tissue-specific glucose kinetics. Glucose infusion rates and measures of whole-body metabolic clearance were greater in DC than in PL or CAF, indicating increased whole-body insulin sensitivity. As the only difference between DC and CAF was the addition of alkaloid caffeine, it can be concluded that caffeine antagonizes the beneficial effects of DC. Given these findings, decaffeinated coffee may represent a nutritional means of combating insulin resistance.
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PMID:Effects of chronic coffee consumption on glucose kinetics in the conscious rat. 1790 93

The prevention of type 2 diabetes has become a major public health objective. Cross-sectional studies have shown a lower prevalence of type 2 diabetes among coffee drinkers. The present article synthesizes results of recent prospective studies, which assessed the relative risk of developing type 2 diabetes according to coffee consumption. Most studies confirm a protective effect against type 2 diabetes, with some dose-response in function of the degree of daily coffee consumption. The observed effect is rather impressive (relative risk reduced to almost 0.70-0.40) and is present whatever the type of population. It appears equal, or event greater, with decaffeinated coffee as compared to regular coffee. These results suggest that the protective effect could not be attributed exclusively to caffeine, but rather that it should be explained by other components, most probably chlorogenic acid and/or various anti-oxidants. The precise mechanism explaining the protection of coffee against type 2 diabetes and its potential relevance in public health remain to be specified.
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PMID:[Does coffee protect against type 2 diabetes?]. 1796 91

With an increasing number of studies describing the negative correlation of coffee consumption and the risk for type 2 diabetes mellitus, we were compelled to elucidate the nutrients which bring pharmacological effects on risk reduction for diabetes. In this review, the author's interest is focused on chlorogenic and caffeic acids derived from lightly roasted coffee beans, as well as nicotinic acid, volatile Maillard reaction products (vMRPs), and another structurally unknown compound contained in heavily roasted beans. Caffeine is a common compound in both lightly and heavily roasted beans and its anti-inflammatory effects on degenerative diseases such as diabetes mellitus has been reevaluated recently. The prophylactic effects of coffee on diabetes involve pleiotropy of plural components in accordance to the degree of the roasting. A new concept of nutritional blended coffee may be important to optimize the prophylactic effects of coffee on lowering the risk factors of diabetes and delaying the progress of diabetes complications as well.
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PMID:[Pharmacological bases of coffee nutrients for diabetes prevention]. 1797 58


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